One of the main causes leading to mortality in diabetes is
myocardial disease. Using
streptozotocin (STZ)-induced diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Interstitial and microvascular disorders are known to be a characteristic part of the
diabetic cardiomyopathy and partly resist
insulin therapy. Because diabetic damage is partly attributed to oxidative stress,
antioxidant treatment may be able to reduce this damage. The aim of this study was to investigate the cardioprotective effect of
sodium selenite, known as an
antioxidant agent. The diabetes was induced by ip injection of 50 mg/kg body wt STZ. The duration of diabetes was 5 wk. The protected group received (ip) 5 micromol/kg body wt/d
sodium selenite (Na2SeO3) over 4 wk following diabetes induction. Electron and light microscopic morphometry of heart samples revealed typical diabetic alterations consisting in an increase in
collagen content, vacuolation, diminishing of the cardiomyocyte diameter, alteration in myofilaments and Z-lines of myofibers, and myofibrillary degeneration.
Sodium selenite treatment could prevent the loss of myofibrills and reduction of myocyte diameter. In the
sodium-selenite-treated diabetic rat heart, alterations of the discus intercalaris and nucleus were corrected, and degenerations seen in myofilaments and Z-lines were reversed by this treatment. Under these findings, one can suggest that
sodium selenite treatment may alleviate late
diabetic complications when it is used under control conditions.